Aging Macaca nigra develop impaired glucose tolerance as a result of a lesion in the islets of Langerhans. The lesion is characterized by appearance of amyloid and occurs concurrently with alteration of secretory cell structure and function. Isolation and characterization of human and monkey islet amyloid protein will allow understanding of the origin of the amyloid. Knowledge of its origin will direct attempts at understanding the causes and at prevention. Antibodies generated with purified amyloid will be used to search for blood markers indicative of the lesion in monkeys and in human beings. Rhesus monkey lymphocyte antigen and protein polymorphisms will be used for phenotypic and genotypic characterization of Macaca nigra. Correlations will be sought between lymphocyte antigen types and the resultant development of diabetes. Establishment of protein polymorphisms will indicate familial interrelationships and make directed breeding possible. Islet cell antibodies may be present as there is islet cell deterioration or may contribute to development of the lesion. Establishment of the assay and longitudinal monitoring will allow correlations between the earliest stages of the islet lesion and the subsequent development of diabetes. Understanding this syndrome in Macaca nigra provides direction for the assessment, prevention, and amelioration of a similar condition in aging human beings.